Previous work has shown that following chronic cardiac denervation or sympathectomy in dogs, the infarct size produced by left anterior descending artery occlusion is dramatically less than in control or acutely denervated hearts. In all previous work infarct size was assessed by the nitro blue tetrazolium method for dehydrogenases. Also, results using tracer microspheres have suggested 2 possible bases of this anti-infarction effect are l) a reduced flow demand in the chronically denervated heart and 2) an increased collateral perfusion. The proposed studies will aid in the further definition and elucidation of this effect. Proposed studies include: (l) Verification of the anti-infarction effect using independent methods for quantifying infarct size. Methods include ST- segment mapping and determination of creatine phosphokinase. (2) Investigation of the effect using other coronary occlusion models such as occlusion of the circumflex artery or its marginal branch. (3) Investigation of regional myocardial perfusion before and after coronary occlusion using tracer microspheres in conjunction with studies of retrograde flow and peripheral coronary pressure in the occluded vessel and antegrade flow in nonoccluded vessels. Both left anterior descending and circumflex occlusion models will be used. (4) Effect of beta-blockade on collateral perfusion and infarct size in the chronically denervated heart. These studies will test the hypothesis that an increased collateral perfusion is due to a supersensitivity to circulating catecholamines in existing collateral vessels. (5) Characterization of oxygen consumption vs ventricular work in the chronically denervated heart. This study will assess the role of a lowered oxygen demand in the anti-infarction effect.